DESCRIPTION: (Applicant's abstract) There is a concern that prolonged beta-amyloid precursor protein expression following injury might actively contribute to the development of Alzheimer-like pathology seen in some survivors of TBI and cerebral ischemia. Thus it is important to understand the conditions under which increased expression of this protein can be modulated so that it does not become toxic to the brain cells. By understanding this mechanism at the cellular level, research- based treatment can be developed to interrupt the processes that lead to the dysfunction and death of neurons after ischemic injury so that recovery, behavioral and anatomical, can be maximized. It is hypothesized that recovery from cerebral can be achieved by manipulating the external environment to modulate the interplay between beta-amyloid precursor protein expression and the molecular responses to injury. In phase one of the study, time course and peak expression of beta-amyloid precursor and molecular responses to injury will be examined in relation to environmental manipulation. In phase two, the effects of modulated levels of beta-amyloid precursor protein aften ischemia on neuronal plasticity and cognitive improvement will be examined.